Related Experiment Videos
ATP-induced Ca2+ signals in bronchial epithelial cells
I Sienaert1, S Huyghe, J B Parys
1Laboratorium voor Fysiologie, K.U. Leuven Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
Pflugers Archiv : European Journal of Physiology
|June 20, 1998
Summary
Respiratory tract chloride secretion relies on calcium signaling. Inositol 1,4,5-trisphosphate (InsP3) receptors, primarily type 3, mediate this calcium release in bronchial cells, with calcium itself modulating receptor activity.
Area of Science:
- Cellular Physiology
- Ion Transport Mechanisms
- Respiratory System Biology
Background:
- Calcium-dependent chloride secretion is vital in the respiratory tract, both in normal function and disease states involving inflammation.
- Understanding the precise mechanisms of intracellular calcium release is crucial for respiratory health research.
Purpose of the Study:
- To investigate the specific mechanisms of intracellular calcium release in immortalized bronchial epithelial cells (16HBE14o-).
- To identify the roles of inositol 1,4,5-trisphosphate (InsP3) receptors and ryanodine receptors in this process.
- To characterize the expression patterns and functional properties of InsP3 receptor isoforms.
Main Methods:
- Experiments on intact and permeabilized 16HBE14o- cells to study calcium release.
- Assessment of InsP3 receptor isoform expression at both mRNA and protein levels.
- Analysis of ATP-induced calcium signals, including calcium spikes and waves.
- Localization of calcium-binding sites within InsP3 receptor isoforms using bacterial fusion protein expression.
Main Results:
- Only inositol 1,4,5-trisphosphate (InsP3) receptors, not ryanodine receptors, were involved in intracellular calcium release.
- InsP3 receptor type 3 showed the highest expression (92.5% mRNA, predominant protein), followed by type 2 (5.4% mRNA) and type 1 (2.1% mRNA).
- Calcium exhibited positive feedback on InsP3 receptors, stimulating release at low concentrations and inhibiting at high concentrations, contributing to ATP-induced calcium signals.
Conclusions:
- InsP3 receptors, predominantly types 3 and 2, are the key mediators of intracellular calcium release in 16HBE14o- cells.
- Calcium-dependent modulation of InsP3 receptor activity plays a significant role in cellular calcium signaling within the respiratory epithelium.
- These findings enhance our understanding of calcium's role in respiratory epithelial function and potential therapeutic targets.